Not AFAIK - I had read Asklipia's post about the different sorts of arabinogalactan and hadn't been able to source the one I wanted so was interested in alternatives. The one I'm after is available in the UK again though so I'll probably go for that (Eclectic Institute's Larix).
The Resistant Starch Challenge: Is It The Key We've Been Looking For?
- Thread starter Ripley
- Start date
Not AFAIK - I had read Asklipia's post about the different sorts of arabinogalactan and hadn't been able to source the one I wanted so was interested in alternatives. The one I'm after is available in the UK again though so I'll probably go for that (Eclectic Institute's Larix).
Something remarkable has happened, and I think it has to be the addition of LAG. I started about mid-July, w/ my probiotics. I'm unable to use fermented food, nor other forms of RS. It seems that in this 6-8 week period something has indeed shifted. For some days now I've needed less potassium, aminos, butyrate, ox bile....and I've been feeling brighter. wow.Frankly, I'm gobsmacked! Less potassium???!!! And even a few times I've self-tested for no probiotics that day. I'm really amazed.
Very interesting, @ahmo! I haven't seen anyone else mention this up until now but I've also noticed that I require less potassium supplementation (actually, electrolytes in general) to stay afloat since starting RS and other prebiotics six months ago. I still can't supplement B12 or 5-MTHF on a regular basis without getting into an untenable potassium situation, though.
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Hi,
I'd suggest you build up your good bacteria with various potent probiotics for a while and try RS again later, or only take 1/2 tsp of RS daily.
I decided to quit RS for now. It was aggravating my GI issues. I'm taking CP1 and Prescript Assist SBOs which should turn my GI tract around sooner or later, enabling me to benefit from RS.
I also have quit eating Ezekiel bread and organic popcorn, which my PHD book says may do me more harm than good.
L
I've found LAG to be somewhat problematic. It has been beneficial, but less so lately. From the beginning, the Swanson FiberAid created a particularly adverse symptomatic response, and it greatly increases inflammation even in very small quantities, so I simply stopped taking this brand. More recently, other brands of LAG seem to act (on me) similarly to acetylcholinesterase inhibitors, which gives me this very unpleasant irritable feeling and mild myoclonic symptoms. I suspect it may be creating a situation whereby the uptake of butyrate is actually inhibited creating a SCFA imbalance of sorts. Anyway, I guess my point is that LAG products are dissimilar in their effects and this prebiotic, and others, might produce variable effects over time, some good, some bad. I am by no means suggesting you avoid this; I actually envision this response changing again as does the ecological community.
Overall, my "tolerance" for other prebiotics is increasing, with fewer adverse effects and more gains. Anyone with ME/CFS is deluding themselves if they do not view this as a multi-year process, but I've taken a huge leap forward with P.E.M., my mood is much more stable, and I am no longer stimulating the flu-like cytokine response as before. I would say I have experienced a significant increase in QOL.
Must admit I'm a bit nervous about trying LAG because it seems medicinal rather than the sort of thing our ancestors would have been eating (trees!). I'm never quite sure if the aim is to restore a healthy gut microbiome or exploit "drug" effects of some of these things. I don't feel as though I've got a good grip of the rationale!
Must admit I'm a bit nervous about trying LAG because it seems medicinal rather than the sort of thing our ancestors would have been eating (trees!). I'm never quite sure if the aim is to restore a healthy gut microbiome or exploit "drug" effects of some of these things. I don't feel as though I've got a good grip of the rationale!
I've only tried Swanson's LAG product but I had to ultimately discontinue it. Initially it provided a very nice energy boost and increased mental clarity (relatively speaking) but after a couple of weeks of taking one 750mg capsule every 2-3 days I noticed unpleasant activation and I seemed to stop being able to sleep. I can't say for sure it was due to LAG but after I discontinued it my sleep gradually returned to "normal" over the course of a few weeks, though they were very scary weeks during which I slept maybe 3-4 hours a night, waking up every few minutes.
Yikes! Thanks for the warning.
Well that is certainly a positive development. This has the makings of enhanced ATP hydrolysis & phosphorylation, which mean your muscles are going to get more glucose and there will be more energy to run those electrolyte transport pumps. I think when this happens you can start correcting the intracellular magnesium deficits. Mg is the dominant +2 cation and your Potassium is never going to come up without Mg. Intracellular hypokalemia is not correctable in the context of hypomagnesemia. Butyrate acts to downregulate Na+/K+-ATPase, the enzyme involved in pumping out sodium while pumping in potassium, which I think underscores the fact that SCFA exerts a positive influence on energy metabolism and electrolytes. These ATPase enzymes are where chemical energy from ATP is transferred to mechanical energy like to drive a transport pump and. There is of course a Magnesium dependent ATPase.
Those methyl donors are circumventing the normal (albeit inhibited in ME/CFS) process of DNA methylation and thus are effectively upregulating gene expression. Eventually, this extrinsic interference (methyl donors) will not have the same adverse consequences. Inhibition of methionine synthase has to exert a protective effect because from what I have seen every really nasty toxin inhibits its activity, but it's effects are at a more fundamental level than methylation. It's one of our many survival mechanisms, I think. Hypermethylation will never prove to be the solution, the rate at which DNA methylation takes place is controlled by energy and redox balance. Although, a little cheating sometimes pays symptomatic dividends.
As an example, another one of those ATP enzymes is H+/K+ ATPase, this is the responsible for acidifying the stomach, it's the proton pump and is of course a target of all those acid-reflux medications. All of these ATP enzymes are globally inhibited, it is clearly concerted. Suppressing the acidification of the stomach limits the availability of proteins and amino acids, and nitrogen metabolites like ammonia and amines. Your ability to process these and use proteins, and not react to them should improve in concert with increases in ATP. Digestive enzymes and stomach acidification thus should be pursued with caution.
For those with gastric reflux, the most problematic foods have something in common--things like chocolate, onions, garlic, coffee, chili powder and other spices, etc. They are very sulfurous and chemically stimulate the cysteine metabolism in the stomach. Proton pump inhibitors work in reverse; they interfere with the proton pump by binding to cysteine molecules. Think of methyl donors doing the same thing, they are circumventing a process,with the real problem only fixed by correcting the redox imbalance.
The bad news is more energy means more detoxification, enhanced immune response, and you've surely got a backlog there. In this respect, it seems one does not get to utilize that energy for her own purposes thus appreciable gains are often not realized, at least immediately. At least that is my rudimentary conceptualization of what happens.
Same thing happens with sleep in those who take acetylcholinesterase inhibitors. AD patients commonly take these, but my experience is with traumatic brain injured patients who use these to promote wakefulness/cognition/memory. It certainly interrupts their sleep and it can't be taken too early in the day. I remember reading about the effects of LAG and recall seeing that its maximal effects on microbial populations is more delayed than I would have expected, 6 hours, perhaps. (I don't remember exactly) Of course this will vary with the product. Perhaps someone has some info on this.
I may have mentioned that I noticed a huge increase in focus with one of my children initially; afterwards, it seemed to provoke exactly what I get...inflammation likely mediated by endotoxin displacement, and an ADHD child to the extreme. Anyway, the sleep interruption like the myoclonus symptoms, I think this is a case of cholinergic hyperstimulation. Did I say I hate this feeling! I believe, potato starch may oppose this somewhat, not sure yet. Of course too much at one time is going to cause adverse effects regardless. The parasympathetic nervous system which is largely regulated by acetylcholine plays a big role in neutralizing the inflammatory response to endotoxins, so the response is also surely related to the "overmobilization" of these bad molecules. Take it slow.
Lou
Senior Member
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I've been taking RS daily(at night) for about ten months now, and I also have far less potassium supplementation need recently. Glad to know Vegas seems to think this may point to some improvement in ATP.
Something else that may bear out what he says is a recent trial of both HCL and digestive enzymes, both of which produced quite negative symptoms.
Something else that may bear out what he says is a recent trial of both HCL and digestive enzymes, both of which produced quite negative symptoms.
I get the exact same thing with larch. Great focus/mental clarity initially, followed by total decompensation - insomnia, agitation, wired feeling. Potato starch has the opposite effect, calming and anxiolytic, at least until the inflammation backlash kicks in. Your acetylcholine explanation makes sense. IIRC, larch increases production of propionate quite a bit compared to other fibers I've looked into (and acetate, but not so much butyrate). Propionate stimulates ACh release in the gut. I take an anticholinergic drug on a daily basis and it helps me a great deal although of course it has its drawbacks when it comes to cognitive function.
I haven't haven't suffered from sensitivity to odors in years, but I have most certainly experienced a huge reduction in sensitivities to foods, which can only be explained by the prebiotics. This spans many categories of offending compounds in foods, wheat/dairy, amine/nitrogen, and aroma compounds. I believe there are a couple of different mechanisms responsible for different sensitivities, but I'm willing to bet that there is overlap between sensitivity to some food chemicals that accounts for the hypersensitivity to odors as they both involve a redox response at the epithelium in the nasal cavity/mouth versus the GIT.
Are you able to tell me what types of food and odors provoke symptoms?
I was hoping for some advice. I have IBS, odd food sensitivities (ie. gluten and some undetermined ones) and what appears to be a very low stomach acid environment (self-diagnosed). Also, have gallstones, though asymptomatic.
I started RS via PS recently. I was able to get to 4Tbs rather quickly without much issue. However, I noticed my stool color lighten and also become loose (and some minor right side achiness). I know an earlier poster mentioned that. In any case, I ceased PS for the moment. It has been a few days and haven't reset yet.
In doing some research, I know H. Pylori and Candida thrive in an alkaline environment, such as the one I have. So, would this be considered die-off? Or am I feeding the bad pathogens? Or is it affecting bile production and aggravating my gallstone situation?
How best to proceed? Should I estart at a much slower doseage and work up slowly?
Thanks.
I started RS via PS recently. I was able to get to 4Tbs rather quickly without much issue. However, I noticed my stool color lighten and also become loose (and some minor right side achiness). I know an earlier poster mentioned that. In any case, I ceased PS for the moment. It has been a few days and haven't reset yet.
In doing some research, I know H. Pylori and Candida thrive in an alkaline environment, such as the one I have. So, would this be considered die-off? Or am I feeding the bad pathogens? Or is it affecting bile production and aggravating my gallstone situation?
How best to proceed? Should I estart at a much slower doseage and work up slowly?
Thanks.
Just about everything I'm afraid. Things like perfume, cleaning chemicals, gasoline are really bad but also "natural" odours like food smells and cut grass.
We have not been able to cook in the house for years due to my sensitivities. Today I managed to eat some canned salmon, but it had to be opened, cleaned and eaten outside. When I'm having a really bad day, I can walk into the kitchen and be overpowered by the smell of a piece of lettuce that someone cleaned to put on their sandwich!
I'm so bad with grass (had IgE allergies to it pre-ME) that I have to stay in a room on the opposite side of the house when the next door neighbour cuts and have aluminum foil covering the furnace grates, room doors closed etc. This with 5 air purifiers going throughout the house!
No one is allowed into the house unless absolutely necessary (i.e.. plumber). When this happens I'm in my room, everything sealed, air cleaner on, towel under door for days. I only come out to gulp down a bit of food and use bathroom.
My food situation is about the same. Right now I'm eating some nuts, Rice chex cereal, almond milk and green tea. Been trying a few fruits since they have been in season but I have something a handful of times, if I'm lucky, and lose tolerance.
My worst problem is severe pain. Excruciating migraines, pain all the way up my nasal passages, nausea, vomiting, sensitivity to sound, light etc. This has been going on for 25 years, I've tried so many things and am getting desperate.
I have tried PS but had problems so stopped. I do seem to be tolerating the Swanson's LAG fine. I started with 1/4tsp FiberAid, increased to 1/2tsp. Added ResistAid 1capsule (500mg). I seem to be handling some smells of unheated foods a bit better. Also getting some stuffiness when exposed to something rather than just a weird reaction like pain or confusion. I hope that means things are shifting back to Th1. I lost my hay fever when the sensitivities appeared.
Didn't mean to make this so long. I just really need something to happen soon.
Wow, it sounds like you have your hands full. I am going to say some things that I expect you will keep in context as being largely hypothetical. I have not studied MCS nor am I trained in chemical sciences.
The only hypothesis that I have seen about the pathophysiology of MCS is the one proposed by Dr. Pall. It does seem that many benefit from his treatment approach of largely using antioxidant compounds to suppress peroxynitrite, superoxide, etc.. I think this suggests there may be some validity to his hypothesis. In my opinion, though, some of the supplements he recommends for purposes of downregulating this NO/ONOO cycle are contraindicated. More consequentially though, this treatment is not likely going to lead to restoration of the underlying pathophysiology. This is similar to Rich's idea's about using methyl donors in ME/CFS. He correctly identified the problem of a redox imbalance with may symptoms certainly created by limited availability reduced glutathione, but I don't think he ever viewed this as a counter-regulatory response.
Like Pall I similarly believe the suppression of these free radicals is fundamental to solving ME/CFS, but I suspect, that many would benefit from treating what I believe to be the source of this problem: the dysbiosis and epithelial dysfunction in the GIT that is maintained by these organisms. Using antioxidants for symptom suppression is likely advantageous and can contribute to recovery; I benefited very dramatically from lipoic acid, which acts at a key point of the metabolism where our energy biosynthesis is undermined. But, I think the restoration of the intestinal epithelial barrier, specifically with the provision of butyrate offers the greatest potential to suppress oxidative and nitrosative stress and correct the aforementioned problems. This is where the battle against these free radicals has to be fought. This is where nitrogen metabolism is deranged, this is where losses in the electron transport chain and glycolysis, etc. take place, these processes are metabolically fundamental.
What I do know about MCS and food sensitivities is that they are frequently, if not nearly universally, co-occuring. I believe this relates to the dysbiotic conditions, particularly at the intestinal epithelium and the explanations but it is important to note that the food sensitivities are not singularly explained.
One thing that happens in ME/CFS is a degradation of the ability to chemically modify our foods. Some food sensitivities clearly relate to the lack of human and bacterial enzymatic capacity to degrade these compounds. In fact, I think there is a parallel and intentional response in loss of energy and secretion of pancreatic enzymes that occurs. Said another way, when we loose the microbes that create enzymes that participate in the breakdown of macronutrients and indigestible or resistant polysaccharides, there is a similar inhibition of our own human digestive enzymatic capacity. We commonly see this when someone is afflicted with severe ME/CFS and starts to develop severe food intolerance, weight loss, fat malabsorption, and obvious pancreatic insufficiency. Think about what this achieves functionally, it suppresses the immune response, which is mediated by many of the compounds and micronutrients contained in our foods. Availability of zinc, fat soluble vitamins A, E, D, & K. This is of course comes with adverse immune consequences, including the creation of antibodies, but I would argue that the higher priority, in the setting of a compromised intestinal epithelium barrier involves suppressing the immune/inflammatory response. As I have studied ME/CFS, I see level after level of ways this has done and the provision of butyrate has a special ability to start to reverse many of these processes unlike anything else I have found.
But there is clearly more to the food sensitivities than poor enzymatic degradation of macronutrients. You can supplement with prebiotics and probiotics and enhance your ability to breakdown these foods, like nurturing organisms with robust amylase enzyme capability to chemically degrade carbohydrates, for example, but this isn't going to correct the energy deficits. I believe many of the food intolerances and the odors that precipitate MCS symptoms relate to particular categories of aroma compounds. What has not been identified, to my knowledge, is that there are organisms that maintain the intestinal epithelium that play specific roles in degrading these compounds. Accordingly, when the ecological community at the intestinal epithelium becomes deranged we simultaneously lose our ability to generate normal energy levels, we stimulate an enormous extra-intestinal inflammatory immune response, we suffer a degraded capability metabolize compounds via the CYP-450 liver enzymes, and very specific compounds utilized by specific organism are no longer efficiently utilized and prove to have toxic consequences. At a cellular level I believe the epithelial dysfunction allows for these chemicals to initiate changes in Nitric oxide and the NOS enzymes that induce these adverse symptoms in the nose/gut/brain that teach us to avoid the offending compounds. NO, iNOS, eNOS play roles critical in maintaining the homeostasis at the intestinal epithelium and also the olfactory cells (in the nose) which transmit odors to the brain.
So if nitric oxide plays an indispensable role in establishing how your brain responds to odors, I think it is reasonable that dysregulation of NO/ONOO contributes to a superphysiological response to odors, but we need to fix the root problem, which is easier said than done.
Take a look at the link and you will see many of the offending compounds. As alluded to above, there are organisms at the surface of the large intestine that have special affinity for some of these compounds. These are highly specialized organisms that can contribute to the metabolism of these compounds while simultaneously contributing to the maintenance of the intestinal epithelium. In fact, I find that these organisms are concentrated at the mucuosal barrier and not in the lumen.
You will see that your old adversary, cut grass, is on this list: cis-3-hexen-1-ol. You seem to have particular sensitivity to aromatic alcohols and probably aldehydes. The better we are able to categorize offensive compounds, perhaps the more likely we are able to find a solution that matches this. You see, there is a reason I have been talking about these chemical compounds for so long. Foods with the highest content of these compounds which create adverse reactions commonly and often proportionately contain resistant polysaccharides,which stimulate the growth of organisms that are most suited to the microbial metabolism of these chemicals. I hope this is not too theoretical for you, but is see a potential role for specific resistant polysaccharides.
Let me know what you think of this list: http://en.wikipedia.org/wiki/Aroma_compound
The only hypothesis that I have seen about the pathophysiology of MCS is the one proposed by Dr. Pall. It does seem that many benefit from his treatment approach of largely using antioxidant compounds to suppress peroxynitrite, superoxide, etc.. I think this suggests there may be some validity to his hypothesis. In my opinion, though, some of the supplements he recommends for purposes of downregulating this NO/ONOO cycle are contraindicated. More consequentially though, this treatment is not likely going to lead to restoration of the underlying pathophysiology. This is similar to Rich's idea's about using methyl donors in ME/CFS. He correctly identified the problem of a redox imbalance with may symptoms certainly created by limited availability reduced glutathione, but I don't think he ever viewed this as a counter-regulatory response.
Like Pall I similarly believe the suppression of these free radicals is fundamental to solving ME/CFS, but I suspect, that many would benefit from treating what I believe to be the source of this problem: the dysbiosis and epithelial dysfunction in the GIT that is maintained by these organisms. Using antioxidants for symptom suppression is likely advantageous and can contribute to recovery; I benefited very dramatically from lipoic acid, which acts at a key point of the metabolism where our energy biosynthesis is undermined. But, I think the restoration of the intestinal epithelial barrier, specifically with the provision of butyrate offers the greatest potential to suppress oxidative and nitrosative stress and correct the aforementioned problems. This is where the battle against these free radicals has to be fought. This is where nitrogen metabolism is deranged, this is where losses in the electron transport chain and glycolysis, etc. take place, these processes are metabolically fundamental.
What I do know about MCS and food sensitivities is that they are frequently, if not nearly universally, co-occuring. I believe this relates to the dysbiotic conditions, particularly at the intestinal epithelium and the explanations but it is important to note that the food sensitivities are not singularly explained.
One thing that happens in ME/CFS is a degradation of the ability to chemically modify our foods. Some food sensitivities clearly relate to the lack of human and bacterial enzymatic capacity to degrade these compounds. In fact, I think there is a parallel and intentional response in loss of energy and secretion of pancreatic enzymes that occurs. Said another way, when we loose the microbes that create enzymes that participate in the breakdown of macronutrients and indigestible or resistant polysaccharides, there is a similar inhibition of our own human digestive enzymatic capacity. We commonly see this when someone is afflicted with severe ME/CFS and starts to develop severe food intolerance, weight loss, fat malabsorption, and obvious pancreatic insufficiency. Think about what this achieves functionally, it suppresses the immune response, which is mediated by many of the compounds and micronutrients contained in our foods. Availability of zinc, fat soluble vitamins A, E, D, & K. This is of course comes with adverse immune consequences, including the creation of antibodies, but I would argue that the higher priority, in the setting of a compromised intestinal epithelium barrier involves suppressing the immune/inflammatory response. As I have studied ME/CFS, I see level after level of ways this has done and the provision of butyrate has a special ability to start to reverse many of these processes unlike anything else I have found.
But there is clearly more to the food sensitivities than poor enzymatic degradation of macronutrients. You can supplement with prebiotics and probiotics and enhance your ability to breakdown these foods, like nurturing organisms with robust amylase enzyme capability to chemically degrade carbohydrates, for example, but this isn't going to correct the energy deficits. I believe many of the food intolerances and the odors that precipitate MCS symptoms relate to particular categories of aroma compounds. What has not been identified, to my knowledge, is that there are organisms that maintain the intestinal epithelium that play specific roles in degrading these compounds. Accordingly, when the ecological community at the intestinal epithelium becomes deranged we simultaneously lose our ability to generate normal energy levels, we stimulate an enormous extra-intestinal inflammatory immune response, we suffer a degraded capability metabolize compounds via the CYP-450 liver enzymes, and very specific compounds utilized by specific organism are no longer efficiently utilized and prove to have toxic consequences. At a cellular level I believe the epithelial dysfunction allows for these chemicals to initiate changes in Nitric oxide and the NOS enzymes that induce these adverse symptoms in the nose/gut/brain that teach us to avoid the offending compounds. NO, iNOS, eNOS play roles critical in maintaining the homeostasis at the intestinal epithelium and also the olfactory cells (in the nose) which transmit odors to the brain.
So if nitric oxide plays an indispensable role in establishing how your brain responds to odors, I think it is reasonable that dysregulation of NO/ONOO contributes to a superphysiological response to odors, but we need to fix the root problem, which is easier said than done.
Take a look at the link and you will see many of the offending compounds. As alluded to above, there are organisms at the surface of the large intestine that have special affinity for some of these compounds. These are highly specialized organisms that can contribute to the metabolism of these compounds while simultaneously contributing to the maintenance of the intestinal epithelium. In fact, I find that these organisms are concentrated at the mucuosal barrier and not in the lumen.
You will see that your old adversary, cut grass, is on this list: cis-3-hexen-1-ol. You seem to have particular sensitivity to aromatic alcohols and probably aldehydes. The better we are able to categorize offensive compounds, perhaps the more likely we are able to find a solution that matches this. You see, there is a reason I have been talking about these chemical compounds for so long. Foods with the highest content of these compounds which create adverse reactions commonly and often proportionately contain resistant polysaccharides,which stimulate the growth of organisms that are most suited to the microbial metabolism of these chemicals. I hope this is not too theoretical for you, but is see a potential role for specific resistant polysaccharides.
Let me know what you think of this list: http://en.wikipedia.org/wiki/Aroma_compound
No, I doubt you are feeding pathogens. Does sound like some immune stimulation. Bile is a finite resource and is fairly conserved, but when you stimulate an immune response you can temporarily decrease its biosynthesis and thus its effect on stool color. Cholesterol 7-alpha hydroxylase, which is rate limiting for bile synthesis, can be inhibited by endotoxins, but there are both positive and negative pressures on bile acid synthesis so it gets a bit more complicated. I think you are just going too fast. Of course I'm not exactly sure what symptoms you are talking about, but a slower pace is likely a prudent step.
"Gassy" may reflect sulfur/sulfate metabolizers, possibly indicative of microbial die-off of a category of organisms predominantly comprised of pathogens.
"Sticky" relates to mucin or mucillage. You have organisms that breakdown mucin (your own) that live just outside the surface of the intestinal tract and they grow at exponential rates when they have resistant starch available to them. A lot of foods that are resistant polysaccharides are preferentially used by organisms to create mucilage because the bacterial organisms secrete exogenous chemicals that can breakdown the polysaccharides to form mucilage. Others have an ability to break down mucin. E.g. Bacillus natto and soybeans-mucilage/several bifidobacterial species and potato starch-mucin.
Think about what happens when you break down a sugar substance that lines the intestinal epithelium.
Cut back substantially and try some other resistant polysaccharides. Based upon your cholinergic symptoms, be careful with LAG.
Vegas, thank you for putting so much time and effort into that long and thoughtful post. You have some very interesting ideas. This definitely gives me something to explore. We are partially veering off-topic yet again so perhaps we might consider starting a related thread. Just not sure where to put it. I'm going to try to summarize what I think you said, just to make sure I haven't misunderstood.
I actually have an idea of what may have triggered the GI problem. It's late so it'll have to wait.
)
Nitric oxide and related enzymes get fouled up. They are critical in both the gut and the olfactory cells and this is why the foods and sensitivities to odours go hand in hand. I should mention that my foods started to go at the same time as my sensitivity to odours began so that fits with your hypothesis. This is the first time I have heard anyone link the olfactory system with the gut mess.
By a combination of avoiding food high in these compounds and supplementing some of these resistant polysaccharides and the specific bacteria they feed, we can hopefully restore the proper balance and banish these sensitivities along with a few other symptoms.
I think I've mostly understood that. At least the general concept. Please correct me if I've gotten something wrong. Will add some other comments tomorrow. Right now I need to get to bed!
You sound like you know more about both than many who supposedly have. And yes, we are just tossing around hypotheticals.
Which supplements do you suspect are contraindicated? I personally haven't had any luck with antioxidants that I have tried thus far. Haven't tried glutathione.
So, if I understand you correctly, you are thinking that the starting point is that the GIT got messed up somehow and fixing the intestinal wall and reducing the free radicals is the best chance at a long term solution. That the Krebs cycle and other key problems can be traced back to gut barrier problems. There are some short term patches that might work but you don't view them as a real solution.
I actually have an idea of what may have triggered the GI problem. It's late so it'll have to wait.
So in addition to problems with leaky gut and food particles venturing into places they should not, we also have a lack of digestion. Either the cause of this cripples both human and microbial abilities to do so, or for some reason we follow the bug's lead or they follow ours if one encounters this issue. And when digestion does not break down things at the very beginning of the cycle, nothing else relating to digestion really goes as it should from then on.
I considered getting some butyrate but couldn't figure out which one as there are several. I also thought I should first see if this could be done with RS and probiotics. Why do you feel butyrate is so superior to other scfa and other products?
You feel the gut wall and dysbiosis problems created a couple, or several large issues that need to be addressed. Digestion of food is one - but only one.
I think you are saying that just as different gut microbes carry out specialized functions in digesting our food they additionally carry out other tasks not usually seen to be related to the digestive process. These include energy, immune and detox functions. Once again the bugs are specialists. (Hey, is this why medicine organized itself into specialties the way it did -- our gut bugs told us how and we just copied their method??
)Nitric oxide and related enzymes get fouled up. They are critical in both the gut and the olfactory cells and this is why the foods and sensitivities to odours go hand in hand. I should mention that my foods started to go at the same time as my sensitivity to odours began so that fits with your hypothesis. This is the first time I have heard anyone link the olfactory system with the gut mess.
I'm getting a bit lost here, but you seem to be suggesting that there are other key substances in or near the gut lining that our gut microbes also act on. If we can figure out which bugs act on which compounds we could then fix, or at least improve, the hypersensitivity issues.
So, foods that contain these compounds usually contain "matching" resistant polysaccharides. This is a grocery delivery for the specific gut bugs these compounds need so that they may be broken down, or digested, so to speak.
By a combination of avoiding food high in these compounds and supplementing some of these resistant polysaccharides and the specific bacteria they feed, we can hopefully restore the proper balance and banish these sensitivities along with a few other symptoms.
I think I've mostly understood that. At least the general concept. Please correct me if I've gotten something wrong. Will add some other comments tomorrow. Right now I need to get to bed!
This is very interesting. My stool was very dark, and I also realize, it is lightening since taking PS. Thank you!
A RS-study:
http://www.vegetablepharm.blogspot.co.at/p/blog-page_9020.html
I also believe, that one must see the treatment of gut as long-term treatment with addressing the gut with a good diet (f.ex. PHD), PS, fibres and probiotics. The gut heals very slow, but ongoing.